Detect and diagnose avascular necrosis in the early stages before treatment options become limited

Detect and diagnose avascular necrosis in the early stages before treatment options become limited

Avascular necrosis (AVN) is a condition affecting bone characterized by cell death, including that of bone marrow, due to a compromised blood supply. Previously, AVN has been referred to by several names including aseptic necrosis, ischemic necrosis, and osteochondritis dissecans. A variety of etiologies have been documented, including trauma, medication use (corticosteroids especially), and organ-transplant recipients; however, by far the most common cause for patients is idiopathic with no known identifiable cause. In idiopathic AVN, the most common sites affected are the head of the femur, humerus, and the metatarsal, distal femurs, and lunate bone.

In these osseous structures, there is a very fragile vascular supply with limited collateral circulation. The peak incidence of idiopathic AVN is between ages 30 and 60. Idiopathic avascular necrosis of the femoral head has a male:female ratio of 4 to 5:1. In 33% to 72% of patients, the disease is bilateral commonly at differing stages of evolution of the process.

Etiology
In the United States, 5% of degenerative joint disease about the hip that require hip replacement are caused by AVN. Occasionally, it can be difficult to differentiate between severe degenerative joint disease and AVN on routine radiography. There is a component of necrosis that has been identifiable in degenerative joint disease, and perhaps the best example of the close association between these two entities is with a condition called rapid destructive coxarthropathy.1 This condition is characterized by dramatic destruction of a previously normal-appearing hip joint over a relatively short time period described by Postel and Kerboull.1

The most common sites of posttraumatic AVN are the femoral and humeral heads, talus, and scaphoid.2 Posttraumatic AVN develops when blood supply is impaired and a function of the relative contributions of the arteries to the bone involved. Hip dislocation may tear the ligamentum teres and the joint capsule, compromising vessels lying in the capsular reflections.

AVN of other causes most often occurs at the hip, followed by the humeral head. Two major theories on the mechanism of action are intraluminal obliteration of end vessels or extraluminal obliteration. There is also an idiopathic AVN at the knee occurring most often in elderly women, which is known as spontaneous osteonecrosis of the knee. However, research3 has pointed toward multiple infractions being the most likely etiology behind this entity.

Clinical Presentation. Patients may present with a wide range of symptoms, such as sudden, severe, incapacitating pain—presumably at the time of initial vascular obliteration and before any bony collapse. At times, symptoms may either be vague or may manifest as biomechanical pain that increases when walking and decreases at rest.

Idiopathic AVN may present as groin pain that intermittently radiates down the anteromedial thigh. Patients may demonstrate an antalgic gait, a gluteus minimus limp, or limited range of motion, especially in flexion, abduction, and internal rotation. A click may be audible when performing the flexion, abduction, and external rotation (FABER) movement. In AVN of the knee, the pain is often sudden and severe and located predominantly over the region of the medial femoral condyle. It can be associated with a “catching” sensation on walking.

Diagnosis. The gold standard for the imaging diagnosis of AVN is currently magnetic resonance imaging (MRI).4 MRI accurately detects the early changes associated with AVN and allows the ability to detect the lesion earlier in its course, and therefore, the treatment may vary accordingly. This is important since with the previous use of routine radiography has led to late detection and limited treatment options, usually resulting in early joint replacement. Bone scintigraphy may also be used since it is sensitive to the reduction of blood supply noted as a photopenic region.

The radiographic signs of AVN are the collapse of the articular surface (most commonly the weightbearing surface), sclerosis, and fragmentation.5 It is possible to develop a subchondral radiolucency representing a subchondral fracture about the femoral head, which is known as the crescent sign.6 With time, the bone revascularises and begins to repair.

Due to the alteration in the morphology of the articular surface, a characteristic shape to the femoral head can occur due to the flattening of the articular surface—this is called the mushroom deformity. Also, because of the alteration in the mechanics about the joint, the large collar osteophyte that develops create a curved radio-opaque region overlying the femoral neck known as the sagging-rope sign.

Complications. Degenerative joint disease is the one of the most common manifestations of AVN complications. This includes the possibility of intra-articular loose body development. More unusual complications involve the evolution of a septic joint and pathologic fracture, as well as the rare and somewhat controversial potential for malignant degeneration noted occasionally in medullary infarcts.

Treatment options. Treatment of AVN patients should begin with avoiding the process in the first instance. The risk of AVN development is a balance that doctors consider when prescribing corticosteroid therapy for a wide range of incapacitating disorders.

Once AVN has been discovered, the best way to prevent long-term joint dysfunction is surgical intervention. Using a classification system designed for MRIs, a technique known as core decompression can be used in the early stages. In this technique, a central portion of bone is drilled out of the femoral neck extending towards the head in an effort to reduce intraosseous pressure and to stimulate revascularisation.

Osteotomies have also been advocated to a lesser degree, whereby there is surgical alteration of the articular surface to redistribute the load-bearing forces. Cortical bone grafts can also be offered to provide additional mechanical support to the subchondral bone to restrict further collapse.

If none of these techniques is effective, the final surgical option is to perform a joint replacement. With the inherent risks of surgery of this procedure, difficulties arise because many AVN patients are young and previously active. The life of the prosthesis is significantly shortened in many cases due to the high level of activity postreplacement, and therefore, these patients may have to undergo a number of these procedures. CP

Michelle Wessely, BSc (Chiropractic), DC, DACBR, FCC (UK/Radiology), is the Departmental Head of Radiology at the Institut Franco-European de Chiropratique, Paris, France. She recently completed the Radiology Research Fellowship at the Department of Osteoradiology, Veterans Affairs Healthcare Center, San Diego, under the direction of Donald Resnick, MD, professor of radiology. Wessely can be reached via email: michelle_wessely@hotmail.com.

References
1. Postel M, Kerboul M. Total prosthetic replacement in rapidly destructive arthrosis of the hip joint. Clin Orthopedics Related Research. 1970;72:138–144.
2. Yochum T, Rowe L. Chapter 13: Hematologic and vascular disorders. Essentials of Skeletal Radiology. 2nd ed. Baltimore: Williams and Wilkins; 1996:1243–1326.
3. Sokoloff RM, Farooki S, Resnick D. Spontaneous osteonecrosis of the knee associated with ipsilateral tibial plateau stress fracture: report of two patients and review of the literature. Skeletal Radiol. 2001;30(1):53-6.
4. Jergesen HE, Heller M, Genant HK. Magnetic resonance imaging in osteonecrosis of the femoral head. Orthopedic Clinics of North America. 1985;16:705.
5. Resnick D. Diagnosis of Bone and Joint Disorders. 6th ed. New York: WB Saunders; 2002.
6. Kenzora JE, Glimcher MJ. Pathogenesis of idiopathic osteonecrosis: the ubiquitous crescent sign. 7hn. 1985;16:681.